Mechanisms of endothelial senescence.
When endothelial cells from different vascular beds are grown in culture they show a limited capacity to divide, eventually entering into a permanent and phenotypically distinctive non-dividing state referred to as 'replicative senescence'. Replicative senescence is thought to result from progressive shortening of telomeric DNA and consequent telomere dysfunction. More recently, it has been realised that senescence can also be induced by a variety of insults, including those causing intracellular oxidative stress. In this report, we review evidence for the occurrence of endothelial cell senescence in vivo. We will also examine the causes, mechanisms and regulation of this process as they emerge from our studies in cell culture, focusing in particular on the roles of oxidative stress, telomerase, growth factors and nitric oxide.
Erusalimsky
Jorge D
JD
Cardiff School of Health Sciences, University of Wales Institute Cardiff, Western Avenue, Cardiff CF52YB, UK. jderusalimsky@uwic.ac.uk
Skene
Chris
C
D002455:Cell Division / Q000502:physiology; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology* / Q000502:physiology*; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D019098:Telomerase / Q000502:physiology; D016615:Telomere / Q000502:physiology
D009569:Nitric Oxide; D019098:Telomerase